The objective of the proposed research is to define mechanisms of host inflammation to schistosomula of Schistosoma mansoni and to examine the role played by the inflammatory process in the rejection of this parasite by immune rodents. It is hypothesized from previous work that the inflammatory response to schistosomula consists of an exudative (monoamine dependent) phase followed by a set of processes causing chemotaxis and adherence of granulocytes to the invading larvae. In the immune host, these nonspecific events are accelerated and augmented by parasite-directed antibodies, an enhancement which results in the reduced survival of challenge schistosomula. Parasite attrition is also governed by the transient susceptibility of developing larvae to immune inflammatory attack. We propose to analyze in detail the mechanisms responsible for the exudation, chemotaxis and adherence of inflammatory cells to schistosomula under both immune and nonimmune conditions and to attempt to identify the processes by which developing schistosomula become refractory to the immune inflammatory response. This work should yield valuable information concerning the effector mechanism of schistosome immunity as well as help to define interrelationships between innate and acquired resistance to helminth infection.